The utility of the agents, currently used to stimulate the failing heart is limited by their toxic effects on the heart or by deleterious side effects on the peripheral circulation. For example, although the cardiac gylcosides are myocardial stimulants and can restore the failing heart, they do so at doses very close to those which produce toxic symptoms of cardiac arrhythmia, nausea and vomiting. The use of sympathomimetic agents are limited by associated arrhythmia, tachycardia, tachyphylaxis or altered peripheral resistance.
The compound of this invention primarily affects the contractile force of the heart muscle. The specific positive inotropic property of AP-C and the accompanying increase in cardiac output make it useful in the treatment of congestive cardiac failure or cardiac arrhythmias.
Anthopleurin-A (AP-A), a cardiotonic peptide obtained from Anthopleura xanthogrammica, has been described in U.S. Ser. No. 710,534, filed Aug. 2, 1976, and Norton et al., J. Pharmaceutical Sciences, Vol. 65, No. 9, 1368-1373, (1976). The present peptide differs substantially from AP-A with respect to the number, composition and sequence of amino acids. The peptide of the present invention is obtained from Anthopleura elegantissima. Anthopleura elegantissima is known to readily reproduce assexually in captivity thus providing an ample and reliable supply of AP-C. Anthopleura xanthogrammica is known not to reproduce in captivity thus the quantity of AP-A available is limited to the amount of anemones which can be harvested from the ocean.